Source:http://linkedlifedata.com/resource/pubmed/id/18647633
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2008-10-16
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| pubmed:abstractText |
In order to examine the effects of alpha3 nicotinic acetylcholine receptor (nAChR) in connection with the pathogenesis of Alzheimer's disease (AD), neuroblastoma (SH-SY5Y) cells were transfected with small interference RNAs (siRNAs) that target specifically towards alpha3 nAChR. The expressions of alpha3 nAChR mRNA and protein were measured by real-time PCR and Western blotting, respectively. The levels of the alpha-form of secreted amyloid precursor protein (alphaAPPs) and total-APP were determined by Western blotting. SH-SY5Y cells transfected with siRNA were then treated with 1muM beta-amyloid peptide (Abeta)(1-42), following which the levels of lipid peroxidation, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the reduction rate of MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] were characterized by utilizing spectrophotometric procedures. As compared to controls, SH-SY5Y cells transfected with siRNA expressed the decreases in the levels of alpha3 nAChR mRNA and protein by 98% and 66% lower levels, respectively; exhibited reduced level of the alphaAPPs; and demonstrated enhanced lipid peroxidation, decreased rate of MTT reduction, and declined activities of SOD and GSH-Px. Inhibited gene expression of the alpha3 nAChR enhanced the toxicity exerted by Abeta. These results indicate that alpha3 nAChR may improve cleavage of APP by alpha-secretase, enhance antioxidation and inhibit the toxicity of Abeta, suggesting that the receptor might play an important role in AD.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Oxidoreductases,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Precursors,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nicotinic,
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (1-42),
http://linkedlifedata.com/resource/pubmed/chemical/nicotinic receptor subunit alpha3,
http://linkedlifedata.com/resource/pubmed/chemical/superoxide reductase
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| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
0197-0186
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
53
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
112-7
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:18647633-Alzheimer Disease,
pubmed-meshheading:18647633-Amyloid beta-Peptides,
pubmed-meshheading:18647633-Cell Line, Tumor,
pubmed-meshheading:18647633-Glutathione Peroxidase,
pubmed-meshheading:18647633-Humans,
pubmed-meshheading:18647633-Lipid Peroxidation,
pubmed-meshheading:18647633-Oxidative Stress,
pubmed-meshheading:18647633-Oxidoreductases,
pubmed-meshheading:18647633-Peptide Fragments,
pubmed-meshheading:18647633-Protein Precursors,
pubmed-meshheading:18647633-RNA, Messenger,
pubmed-meshheading:18647633-RNA, Small Interfering,
pubmed-meshheading:18647633-RNA Interference,
pubmed-meshheading:18647633-Receptors, Nicotinic
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| pubmed:year |
2008
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| pubmed:articleTitle |
Inhibiting gene expression of alpha3 nicotinic receptor in SH-SY5Y cells with the effects on APP metabolism and antioxidation in Alzheimer's disease.
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| pubmed:affiliation |
Department of Pathology and Molecular Biology, Guiyang Medical University, Guiyang 550004, Guizhou, PR China.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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